Why is myxedema coma named as such, particularly in older adults with a history of untreated or undertreated hypothyroidism?

Why Myxedema Coma is Named "Coma"

Myxedema coma is named "coma" because altered mental status progressing to coma is the defining clinical feature of this life-threatening endocrine emergency, even though not all patients present in frank coma. The term reflects the most severe neurological manifestation of profound hypothyroidism, where the brain's metabolic demands cannot be met due to critically low thyroid hormone levels.

The Clinical Definition and Neurological Features

The term "myxedema coma" describes the extreme manifestation of hypothyroidism characterized by altered mental status as its cardinal feature 1. While "myxedema" refers to the non-pitting edema that occurs in severe hypothyroidism 2, the "coma" component specifically denotes the profound neurological dysfunction that defines this medical emergency 3.

Altered mental status is the critical diagnostic criterion, ranging from confusion and lethargy to frank coma 4, 1. The neurological impairment occurs because:

• The brain's metabolic demands cannot be met with critically low thyroid hormone levels
• Cerebral hypoperfusion results from the profound hemodynamic instability 5
• Hypoventilation leads to hypercarbia, which further depresses consciousness 3
• Severe hyponatremia contributes to encephalopathy 1

Why "Coma" Despite Variable Presentations

The term "coma" persists even though not all patients present in frank coma because it emphasizes the life-threatening nature and the potential for rapid neurological deterioration 1. Patients may present with:

• Confusion and disorientation as initial manifestations 4
• Progressive lethargy advancing to stupor 1
• Complete unresponsiveness in the most severe cases 3

A 7-year-old patient with central hypothyroidism presented with altered mental status and returned to baseline activity within 48 hours after treatment, demonstrating that the "coma" can be reversible with prompt intervention 3. Similarly, a 47-year-old woman with subclinical hypothyroidism developed hypothermia, circulatory collapse, and coma, responding dramatically to intravenous T3 therapy 6.

The Pathophysiology Behind the Neurological Collapse

The progression to coma occurs when homeostatic mechanisms compensating for chronic hypothyroidism are overwhelmed by precipitating factors 1. These precipitating factors include:

• Surgery and trauma as major physiologic stressors 7
• Infection triggering metabolic decompensation 1
• Sedatives and anesthetics that further depress consciousness 8
• Hypoglycemia requiring immediate correction 7

The neurological deterioration reflects multiple organ system failures:

• Cardiovascular collapse with bradycardia, hypotension, and reduced cardiac output compromises cerebral perfusion 4, 1
• Respiratory failure with hypoventilation causes hypercarbia and hypoxia, both depressing consciousness 3
• Metabolic derangements including hyponatremia, hypoglycemia, and metabolic acidosis directly impair brain function 6, 4

Historical Context and Clinical Reality

Myxedema coma remains a diagnostic challenge due to its rarity, but the term "coma" serves as a critical warning to clinicians about the severity and urgency of this condition 5, 1. The mortality rate remains high despite modern treatment, making prompt recognition essential 4, 1.

The term accurately reflects that this is a true medical emergency requiring immediate intensive care 5, 1. Emergency physicians must anticipate potentially difficult airways due to posterior pharyngeal angioedema, even when external facial edema appears benign 5. Patients require:

• Immediate admission to intensive care units 1
• Vigorous pulmonary and cardiovascular support 1
• Intravenous thyroid hormone replacement (levothyroxine preferred over liothyronine) 8, 1
• Simultaneous glucocorticoid administration until adrenal insufficiency is excluded 8, 1

The "coma" designation emphasizes that altered mental status is not merely a symptom but the defining feature that distinguishes this life-threatening emergency from severe hypothyroidism without neurological compromise 3, 4. Even in the rare case of myxedema coma occurring with subclinical hypothyroidism (normal free T4 and T3 but elevated TSH), the altered mental status and coma were the presenting features requiring emergency intervention 6.